Abstract
During the 1971 epidemic of Venezuelan equine encephalomyelitis (VEE) in S Texas [USA], 203 suspect VEE cases were evaluated by the Center for Disease Control; 67 were confirmed as cases of VEE. Laboratory confirmation was accomplished by isolatno of VEE virus from a serum specimen taken during the acute illness in 50 (75%) of the confirmed cases. Serological confirmation was obtained in 17 cases (25%). Virus isolations were most often obtained from sera collected during the first 3 days of illness. Peak serum virus titers (algebraic mean, 105.7 suckling mouse intracranial 50% lethal doses [SMICLD50]/ml) occurred on day 2 of illness. Of the sera from which virus was isolated, 1/2 contained at least 105 SMICLD5-0/ml, which is sufficient to infect some vector mosquitoes. Blood from 13 virus-positive VEE cases was obtained 1 and 11 mo. after illness. Hemagglutination-inhibiting, complement-fixing and neutralizing antibodies were formed by all 13 patients 1 mo. after illness. Hemagglutination-inhibiting antibody titers were essentially unchanged 11 mo. after illness. Complement-fixing antibody was undetectable 11 mo. after illness in 23% of cases and was detectable at dilutions of 1:8 or 1:16 in 77%. Neutralizing antibody (measured by log neutralization index) was not detectable 1 yr after illness in 1 person (8%); titers declined from 1.0-2.0 in 46%, were unchanged in 39%, and were not tested in 1 person (8%). No evidence of intrafamilial spread of VEE virus was obtained in 2 illness and antibody surveys. A randomized household illness and antibody survey of 681 Port Isabel residents revealed an inapparent infection ratio of 1:11 and an overall antibody prevalence of 3.2%.